okay so welcome to another MedCram
lecture we're going to talk about acute
renal failure and for that when we sort
of bring up our chem seven again we
talked about this before you remember
you'll see this a lot it's standard we
have sodium you've got potassium you've
got chloride you've got the bicarb and
we could talk about the B UN the
creatinine okay so that's this third
column bu when should we refer to as the
B you I never call it the bun it stands
for the blood urea nitrogen okay blood
urea nitrogen and the C R is simply
creatinine okay so blood urea nitrogen
and creatinine so these things have to
do with acute renal failure but let's
get into a little bit about what they
are and where they came from and as you
know when you're talking about energy
you remember something from biochemistry
called the Krebs cycle Krebs cycle okay
and it goes around and around and you
remember what went into it first there's
this thing called acetyl co a okay and
it was basically two carbons when it to
ask Toa and what came out of Krebs cycle
ATP you know you had these reducing
agents nadh fadh2 they went into a
electron transport chain down the
electron transport chain and you got ATP
okay so basically you need to have two
carbon units to get into this Krebs
cycle well let's talk about what are the
three different types of energy sources
in the body there's three types we know
that there's carbs okay and carbs are
usually six carbon chains and six carbon
chains get broken down into two times
three carbon chains and then remember
one of these carbons comes off in the
form of co2 during glycolysis and then
you've got a two carbon chain and boom
you're ready to enter Krebs cycle
the other one is fats or lipids okay you
remember that it had the carboxylic and
on it and you had a bunch of these
carbons that went off it was 16 carbons
then it's palm mathilde koay and then
remember beta-oxidation it chops these
thing
in - guess what - carbon units you're
able to enter into Krebs cycle well the
last energy group is you guessed it
proteins proteins if you recall is a
collection or a string of amino acids
which have the backbone of n C C and
then you have another n c c well you
would have protease is that are chopping
up these proteins they're chopping them
up into these NCC units these are amino
acids how do you get these NCC s to C
C's well you basically chop off this n
group and then boom you've got C C's
going in and you can make ATP the
problem is is that there's these ends
that are left behind so what are these
ends these ends are something called
ammonia or nh3 okay
so we got to get rid of these NH 3
groups well these NH 3 groups ammonia as
what it's known as okay ammonia is toxic
to the body it's toxic to the brain if
you have too much of it it can cause
hepatic encephalopathy so the body's got
to do something about it somehow to get
rid of it and that's where we talk about
the BU n ok so clear the screen here
we've got nh3 which is ammonia and nh3
goes to the liver okay here's my picture
of the liver so it goes into the liver
and what comes out is something that
looks like this C double bond o wooden
to the nh3 or NH 2 on one side and an NH
2 on the other
this is urea okay you are e a it goes
into the blood then you get blood urea
nitrogen so the nitrogen is now
compounded this is not as toxic so this
is really nice to have because you can
excrete this through the kidney so again
ammonia goes to the liver and then gets
made into your wreath through something
called the areia cycle which we won't
get into and then you get this bu n now
bu n blood urea nitrogen goes to the
kidney
okay there's my little picture of the
kidney and it goes out and that's how
you get rid of be went so we know how
that happens now let's talk a little bit
about bu and remember a first point is
this it's made in the liver okay and
there are a couple of things that have
absolutely nothing to do with the
kidneys that could increase the amount
of bu n that you measure in the blood
first of all let's talk about burns so
burns is a catabolic state what do you
what do you think is gonna happen when
you have a burn burns are gonna cause
you to have more protein breakdown as we
already know more protein breakdown is
going to give you more ammonia all right
what about steroids
again steroids induces a catabolic state
accountable like state is going to give
you more breakdown of proteins that's
gonna give you more ammonia livers gonna
make more urea what about certain
antibiotics
tetracycline okay so here is tetra SCI
clean burns can do it and steroids
catabolic state okay all of these things
can do it let's think about something
else let's say you've got liver problems
now in liver problems or liver failure
or cirrhosis you can get esophageal
varices esophageal varices is basically
situation where blood is trying to get
back to the heart through the liver the
livers dysfunctional and because of that
the blood has to find an alternative
route back to the heart and one of those
ways is through the esophagus so these
tiny veins which are normally built only
to take so much blood become engorged
and so these veins can burst and high
mortality high mortality associated with
this so you've got bleeding
what is bleeding bleeding into the into
the digestive tract well when that
happens you've got these red blood cells
okay red blood cells are full of globin
globin is a protein you digest down all
this protein guess what you're gonna get
you're gonna get ammonia well you
already have liver failure so you're not
making this urea and so what's get a
skyrocket your ammonia levels going to
skyrocket and that's why we see in
patients with liver failure who have
bleeding
hijole bleeding they get hepatic
encephalopathy and in fact that's how
you can tell they're having a patek
encephalopathy now let's say that they
have a GI bleeding and it's not due to
liver failure if their livers working
just fine you won't see a buildup of
ammonia but in fact the liver will take
that ammonia and guess what you're gonna
have an increase in you're gonna have an
increase in the B um so you can have an
increase in your bu n if you have GI
bleeding and your liver is working what
are some things that could cause your bu
n to be decrease so all of these things
cause your bu n to go up okay what are
some things that could cause your bu n
to go down well the obvious thing is
this your livers not working because if
your livers not working you're not gonna
make bu n and so liver failure I see
this all the time patients come in with
liver failure and I'll look on the
chem-7 and their bu n is pretty low
sometimes it's really even undetectable
okay so we've talked about bu and let's
review that again it's synthesized in
the liver things that increase it that
have nothing to do with the kidney would
be fever catabolic state GI bleeding
tetracyclines
all sorts of things things that decrease
that would be liver failure because it
can't make the BU n okay with all those
things in mind let's talk about what
we're talking about today which is
kidney failure so I'm gonna draw a
nephron here's my little stylized
nephron okay this is remember the kidney
works kind of like you should clean out
your closet you take everything out of a
closet everything and then you put back
just the stuff that you want to keep and
everything else gets thrown away so
here's the nephron and here is the blood
supply so you have the afferent
arteriole going in and the efferent this
is a bunch of capillaries and what you
have is you've got flow of fluid into
Bowman's capsule or the glomerulus and
things go down and basically everything
that you want to keep gets reabsorbed
and what get what is left gets dumped
out into the toilet okay but remember
stuff that you want to keep gets
reabsorbed and most of the stuff that
gets reabsorbed gets read
absorbed right here at something we call
the proximal convoluted tubule probably
70% of the stuff that gets reabsorbed
gets reabsorbed here at the proximal
convoluted tubule so about 70% of stuff
here in the proximal combo to it gets
reabsorbed and so really there's two
things that you've got to be aware of
that effect the serum concentration of
things in the serum so if things here
are being reabsorbed back into the serum
and those two things are is the GFR the
glomerular filtration rate what is the
rate at which stuff is being filtered
into Bowman's capsule if you've got
acute renal failure this is going to be
reduced and therefore if less for
instance if less B UN is being filtered
into Bowman's capsule you're gonna have
an increase in your B UN outside that
goes for just about anything that's
being filtered the less filtration rate
the greater that accumulation is going
to be in the serum because it's just not
being filtered but there's an extra
added thing here with bu in and that is
is that once it gets filtered if this
GFR or this glomerular filtration rate
is low it's going to go along here some
more slowly and if it goes along here
more slowly it's more likely to be a
reabsorbed because B UN is specifically
reabsorbed here at the proximal
convoluted tubule so there are in fact
two reasons why the B UN would go up in
a low GFR situation number one it's
because it's not being filtered at the
same rate and the stuff that is being
filtered is more likely to be reabsorbed
that's going to become very important
later on now this is a contra
distinction to something called
creatinine we'll talk about creatinine
cratan basically comes from muscle but
specifically creatinine is also filtered
here at Bowman's capsule but it is not
reabsorbed it just keeps going through
and right on out in fact there are areas
here where creatinine is actually
actively secreted
okay so what does that mean that means
that if there is a low glomerular
filtration rate that's a reason why
creatinine is going to go up but it's
not going to have the other reason to go
up because it's not being actively
reabsorbed in fact it's being secreted
and so creatinine only goes up for one
reason in a low GFR state that's the
major difference there between
creatinine and the B UN let's talk a
little bit about creatinine what is
creatinine okay
creatinine again and the chem-7 is this
area down here and where does it come
from it comes from muscles so muscle
breakdown is going to give you
creatinine that's just a natural
byproduct so the more muscle you have
the higher your correcting is going to
be normally and the less muscle you have
the less your Kratt name is going to be
and typically you need to see a
reduction in your GFR by at least 50
percent before you see an increase in
your creatinine so what are some non
renal things that could increase Kratt
knee and things that have absolutely
nothing to do with the GFR well as we
talked about remember there are areas
here in the nephron specifically where
creatinine is secreted if you could take
a inhibitor of that and block it you
would block the secretion of cranny that
would increase your serum concentration
of creatinine and there are a couple of
drugs that do that one of them is called
cimetidine tagamet it's an h2 blocker
and the other one is an antibiotic
called trimethoprim okay so you'll see
an increase in crowding for that what
about decreased cracking what could
cause a decrease in creatinine we talked
about profound muscle wasting so low
muscles so if you don't have any muscles
that would cause you're creating to go
down and that would be a reason for your
Kratt need to be low okay so to review
remember bu and is synthesized in the
liver
it is both reabsorbed it is filtered and
reabsorbed the creatinine is filtered
and secreted it is not really
so if there is a slowdown in filtration
the BU n is going to be increased
because of lack of filtration and also
because of reabsorption the cratan is
only going to be increased because of
lack of filtration therefore you're
going to see a larger bu n increase than
you would creatinine in a low flow state
all right that does it for part 1 join
me for part 2